Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male Sprague-Dawley rats were treated with a single i.p. injection of DMSO (3.0 ml/kg) or 9-nitrophenanthrene (9-NP, mg/kg) in DMSO. 9-NP produced a significant elevation of serum aspartate aminotransferase, alanine aminotransferase, sorbitol dehydrogenase, and gamma-glutamyl transpeptidase (GGTP) levels relative to DMSO-injected rats 24 hr after injection. With the exception of GGTP, the increase in enzyme activities induced by 9-NP was significantly reduced by a 3-day pretreatment with beta-naphthoflavone (BNF; 40 mg/kg/day) in DMSO. The effect of 9-NP on GGTP levels was enhanced by BNF pretreatment.
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PMID:Toxicity of aromatic hydrocarbons. VII. Hepatotoxicity of 9-nitrophenanthrene, and protection against it by beta-naphthoflavone. 290 38

Patients with proximal stomas or high fistulas and defunctionalized intestine who are receiving total parenteral nutrition (TPN) often develop hepatic enzyme abnormalities and hyperbilirubinemia. A technique was developed to collect intestinal secretions from proximal stoma and to reinfuse these secretions into the distal part of the intestine. This technique was applied in eight patients with a disrupted intestinal tract. A significant decrease (p less than 0.05) in elevated serum bilirubin, alkaline phosphatase and gamma-glutamyl transpeptidase levels was observed. Alanine aminotransferase and aspartate aminotransferase levels did not change significantly. The plasma sodium levels, slightly subnormal before reinfusion (131.0 +/- 4.6 millimolar per liter), despite enormous supplementation, normalized during reinfusion (137.0 +/- 4.0 millimolar per liter). TPN was continued during this infusion. This suggests that TPN by itself does not cause intrahepatic cholestasis. Neither could it be explained by an effect of secondary bile acids because these were most likely not produced as bile did not reach the distal defunctionalized intestine. Three possible mechanisms are suggested. Restoration of passage in the distal intestine may diminish bacterial overgrowth, endotoxin production and absorption. Enlargement of the bile acid pool may diminish the susceptibility of the liver to the deleterious effects of endotoxins. We advocate this reinfusion technique to overcome the metabolic disturbances occurring in those patients with high-output stomas or fistulas arising from the proximal parts of the small intestine.
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PMID:Reinfusion of secretions from high-output proximal stomas or fistulas. 290 95

Cyclosporine blood levels were measured in 225 blood samples taken 14 days to 3 years after transplantation from 8 adult and 7 pediatric liver graft recipients. Results by high-performance liquid chromatography, radioimmunoassay with a polyclonal antibody (PARIA) or with a selective monoclonal antibody (MARIA) were compared in the context of major clinical events and alterations in serum bilirubin, aspartate aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, urea, and creatinine. Cyclosporine blood levels by MARIA were significantly higher than HPLC values, but only by mean values of 11 micrograms/L in adult and 20 micrograms/L in pediatric patients. These differences were unaffected by alterations in liver or renal function and seem unlikely to affect clinical management. Minimum PARIA:HPLC ratios of 2-4 were noted in patients with good graft function, with higher ratios (up to 18) associated with hepatic dysfunction. Multiple regression analysis demonstrated that elevations in serum bilirubin and alkaline phosphatase significantly contributed toward the correlation with raised PARIA:HPLC ratios in adults and that gamma-glutamyl transpeptidase and aspartate aminotransferase were additionally important in children. There was no significant contribution from either serum urea or creatinine levels to raised PARIA:HPLC ratios, but in children a positive correlation existed between these indicators of renal function and trough cyclosporine concentrations determined by selective methods (HPLC and MARIA).
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PMID:Cyclosporine blood levels--an evaluation of radioimmunoassay with selective monoclonal or polyclonal antibodies and high-performance liquid chromatography in liver transplant recipients. 305 89

Hepatic function can be monitored using exogenous (e.g., sulfobromophthalein, indocyanine green, antipyrine, aminopyrine, galactose) and endogenous substances (e.g., bile acids, PT/PTT, albumin, ammonia, bilirubin). Test of hepatic necrosis include aspartate aminotransferase, and alanine aminotransferase. The hepatobiliary system can be assessed using alkaline phosphatase, 5'-nucleotidase, gamma-glutamyl transpeptidase, ultrasound, and iminodiacetic acid scans.
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PMID:Monitoring hepatic function. 306 53

Real-time ultrasonography (US), computed tomography (CT), and biochemical tests were prospectively performed to detect gallstones in 88 consecutive patients immediately after the onset of an attack of acute pancreatitis. The sensitivity of biochemical tests was 84.6% when the patients had three or more positives of five parameters [including serum bilirubin, alkaline phosphatase (AP), gamma-glutamyl transpeptidase (GGT), alanine transaminase (ALT), and alanine transaminase-aspartate transaminase (ALT-AST) ratio]. The sensitivity, specificity, and accuracy were 71.8, 98.0, and 86.4% for US, and 52.9%, 100%, and 79.5% for CT. The sensitivity, specificity, and accuracy were improved to 82.1, 100, and 93.2% by the combination of US and CT, and 94.9, 100, and 97.7% by the combination of US and biochemical tests. Adding CT to the combination of US and biochemical tests resulted in only a slight improvement in sensitivity and accuracy. In conclusion, a combination of US and biochemical tests can provide the best noninvasive method in rapidly detecting gallstones as an etiological factor in acute pancreatitis. Computed tomography is not cost-effective. A positive result of biochemical tests despite a negative finding in US calls for an intensive search for gallstones by further investigation with endoscopic retrograde cholangiography or repeated US examinations.
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PMID:Clinical significance of ultrasonography, computed tomography, and biochemical tests in the rapid diagnosis of gallstone-related pancreatitis: a prospective study. 328 69

The hepatotoxicity of a new erythromycin derivative, erythromycin acistrate (EA, 2'-acetyl erythromycin stearate), was compared with that of erythromycin stearate (ES), erythromycin estolate (EE) and erythromycin-11,12 cyclic carbonate (EC) in 4-5-day, 28-day and 6-month oral toxicity studies in rats and dogs. In the 4-day rat study, EC caused fatty metamorphosis in the liver. ES caused similar, but milder changes at a dose nearly five times higher. The 5-day dog study revealed markedly increased serum alanine aminotransferase (S-ALAT), serum aspartate aminotransferase (S-ASAT), serum alkaline phosphatase (S-APHOS) and serum gamma-glutamyl transpeptidase (S-gamma-GT) values in the EC- and EE-groups, and slightly elevated S-ALAT values also in the EA- and ES-groups. Microscopy revealed cholangitis, pericholangitis and phlebitis in the portal areas in the EC-group at all doses. Epithelial hyperplasia was observed also in the bile ducts. EE caused similar but milder changes. The changes in the EA-group were small, but mildly atypical bile duct epithelium was seen in female dogs receiving 2 x 200 mg/kg of EA. The ES-group was practically without changes and very much like the EA-group. Thus the dog proved to be a more sensitive model for assessing the hepatotoxicity of erythromycin derivatives. In the 28-day studies, only EA and ES were investigated. In the rat study, slightly elevated serum enzyme levels within the normal range were measured in the high-dose regimens of both drugs. In the dog study, 300 mg/kg of EA caused slightly elevated S-ALAT in males, but the values returned to normal after a 2-week off-dose period. Only EA was studied in the 6-month study. In male rats, 400 mg/kg of EA caused slightly elevated enzyme levels and neutral fat droplets in centrilobular hepatocytes. In male dogs given 150 mg/kg of EA, S-ALAT, S-APHOS, and S-gamma-GT values were elevated after four weeks of treatment but returned to normal thereafter. No severe changes were seen in the liver histopathology. In conclusion, EC and EE were clearly hepatotoxic in dogs, and EC also in rats. EA, and to a somewhat lesser extent ES, showed signs of mild hepatotoxicity only at high doses. This evidently reversible effect was considered a common characteristic of erythromycins.
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PMID:Comparative liver toxicity of various erythromycin derivatives in animals. 233 25

In order to establish sensitive methods of detecting minor renal damage, changes of enzymes, tubular cell counts, and creatinine in the urine were investigated in rats that had been given nephrotoxic chemicals. Daily administration of mercuric chloride (HgCl2) dose-dependently increased urinary excretions of lactate dehydrogenase (LDH), aspartate aminotransferase (GOT), alkaline phosphatase (ALP), leucine aminopeptidase (LAP), lysozyme (LZM), N-acetyl-beta-D-glucosaminidase (NAG), and acid protease together with increased counts of tubular cells in the urine. The increase in tubular cell counts and the change in urinary LDH isoenzyme profile preceded the changes in the other enzymes. Daily administration of gentamicin (GM) increased urinary excretions of LDH, GOT, LZM, NAG, acid protease and tubular cell counts in a dose-dependent manner, but did not increase gamma-glutamyl transpeptidase (gamma-GTP) and ALP excretions. The urinary isoenzyme profiles of LDH in rats treated with GM were different from those with HgCl2. The increase in acid protease excretion outlasted those in LDH and GOT in the high dose group. It was concluded that the severity of renal damage can be readily detected by periodic determinations of the following urinary parameters: tubular cell counts, LDH isoenzyme, acid protease, LZM and NAG, in addition to either LDH or GOT and one of the enzymes ALP, LAP or gamma-GTP. Furthermore, the site of renal damage can be presumed from these results.
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PMID:Urinalysis for detection of chemically induced renal damage (1)--Changes in urinary excretions of enzymes and various components caused by mercuric chloride and gentamicin. 344 39

In order to establish sensitive methods of detecting minor renal damage, changes of enzymes, protein, tubular cell counts, and creatinine in the urine were investigated in rats to which nephrotoxic chemicals had been administered. Daily administration of p-aminophenol (PAP) dose-dependently increased urinary excretions of lactate dehydrogenase (LDH) and its isoenzymes (LDH5 = LDH4 greater than LDH3 greater than LDH2 = LDH1), aspartate aminotransferase (GOT), alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (gamma-GTP), leucine aminopeptidase (LAP), lysozyme (LZM), N-acetyl-beta-D-glucosaminidase (NAG) and acid protease together with increased counts of tubular cells in the urine. Tubular cell counts, LDH and GOT were more sensitive indicators in the PAP tubulonephritis. Single i.v. injection of puromycin aminonucleoside (PM) dose-dependently increased urinary excretions of LDH and its isoenzymes (LDH1 = LDH5 greater than LDH2 = LDH4 greater than LDH3), GOT, NAG, acid protease and protein but degree of the increases in these enzymes was lower than those in the rats treated with PAP. PM increased excretions of high molecular weight proteins but did not increase ALP, gamma-GTP, LAP, LZM and tubular cells excretions. Single i.v. injection of hexadimethrine increased urinary excretion of LDH and its isoenzymes (LDH1 = LDH5 greater than LDH2 greater than LDH3 = LDH4), GOT, LZM, NAG and acid protease together with increased counts of tubular cells in the urine but did not increase ALP, gamma-GTP and LAP excretions. It is concluded that tubular cell counts, LDH isoenzymes and battery of these enzymes in urine are useful markers for detecting the severity and the site of renal damage in addition that urinary protein is a useful marker for detecting glomerular damage.
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PMID:Urinalysis for detection of chemically induced renal damage (2)--Changes in urinary excretions of enzymes and various components caused by p-aminophenol, puromycin aminonucleoside and hexadimethrine. 344 40

Male Sprague-Dawley rats were treated ip with beta-naphthoflavone (BNF, 40 mg/kg/day) in dimethylsulfoxide (DMSO, 26.7 mg BNF/ml) for three days. At 24 hr after the pretreatment DMSO (3.0 ml/kg), phenanthrene (150 mg/kg), ozonized or nitrated products of phenanthrene (150 mg/kg), pyrene (150 mg/kg), or ozonized or nitrated products of pyrene (150 mg/kg) were injected ip. Phenanthrene, pyrene, and their ozonized or nitrated products were dissolved in DMSO (50 mg/ml). No increase in the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT) or sorbitol dehydrogenase (SDH) was seen in the pretreated rats 48 hr after the treatment. This is in contrast to what was seen in previous work without the BNF pretreatment. BNF pretreatment induced a small but significant increase in gamma-glutamyl transpeptidase (GGTP) levels. No treatment group receiving BNF differed from another with respect to GGTP. A decrease in lactate dehydrogenase (LDH) levels was noted in the nitro-PAH treatment groups; the same phenomenon was observed earlier in rats treated with nitro-PAH without BNF treatment. These results suggest that the mixed-function oxidase systems specifically induced by BNF have a protective effect against the hepatotoxicity of the oxonized or nitrated products of phenanthrene and pyrene.
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PMID:Toxicity of polycyclic aromatic hydrocarbons. III. Effects of beta-naphthoflavone pretreatment on hepatotoxicity of compounds produced in the ozonation or NO2-nitration of phenanthrene and pyrene in rats. 357 42

To characterize the incidence and severity of liver function abnormalities in patients with congestive heart failure, we analyzed systemic hemodynamics and biochemical profiles in 133 patients with stable chronic congestive heart failure, secondary to a dilated cardiomyopathy. The patients were divided into three groups, based on the severity of the reduction in cardiac index (CI). The mean values of all liver function tests in groups 1 (n = 43; CI greater than or equal to 2.0 L/min/m2) and 2 (n = 48; CI greater than 1.5 and less than 2.0 L/min/m2) were essentially normal, except for minimally elevated alkaline phosphatase levels and slightly decreased albumin levels in both groups, and slight increases in levels of gamma-glutamyl transpeptidase and total bilirubin in group 2. In contrast, group 3 patients (n = 42; CI less than or equal to 1.5 L/min/m2) had the most severe heart failure, as assessed by the lowest CI and highest cardiac filling pressures, and significantly higher levels of aspartate aminotransferase (65 +/- 82 U/L), alanine aminotransferase (77 +/- 102 U/L), lactate dehydrogenase (282 +/- 91 U/L), and total bilirubin (29 +/- 14 mumol/L [1.7 +/- 0.8 mg/dL]). The percentage of patients in group 3 with these abnormalities ranged between 27% and 80%. Although linear regression analysis showed that the elevations in right atrial and pulmonary wedge pressures, and the decreases in CI, were significantly correlated with liver function abnormalities, the correlation coefficients were small. Thus, liver function abnormalities remain common in patients with congestive heart failure but are generally small in magnitude and not associated with clinically apparent hepatic disease. It is likely that reduced forward flow and passive backward congestion are both contributing factors in the pathogenesis of these biochemical abnormalities, although nonhemodynamic factors may also be important.
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PMID:Liver function abnormalities in chronic heart failure. Influence of systemic hemodynamics. 360 80


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